Ambient Particles Instilled in People at Very Low Doses Cause Airway Inflammation

BrooklynDodger repeatedly points to the burst of research findings showing adverse health effects of ambient air particle pollution at levels of exposure permitted by EPA limits. The Dodger has argued that mass of small particles or particle count – both available in real time by direct reading instruments – is the best measure, certainly the most convenient. Particles with no special toxicity – carbon black, amorphous silica – appear equally potent in animal systems to diesel particulate matter, and much more potent than cigarette smoke. Expensive chemical analysis only gets in the way, and opens the field to special pleading and Houdini risk assessments.

Nevertheless, the Dodger concedes that chemical composition could be a modifier or intensifier of the effect. Metal particles in the air are expected to be oxides generate from combustion products; PM 2.5 particles are expected to be agglomerations of smaller particles immediately generated by combustion. Cadmium oxide, chromium (VI) oxide are plausibly more potent carcinogens [now the Dodger has to look this up.] Iron oxide – probably the most weighty of these metal compounds – can be thought of as delivering oxidative power in concentrated form to the cell membranes of the respiratory system.

The Dodger reminds readers that these exposure levels are much less than typically encountered in the workplace.

The paper summarized below is premised on a connection between tissue damage to the respiratory system and asthma, which may be incorrect. However, it demonstrates the potency of particles concentrated from ambient air, and suggests greater potency for metal rich particles:

Investigators compared effects of particles from a German smelter area known to have increased asthma in children to a non-industrialized area…100 µg of PM2.5 suspensions, collected simultaneously in the two areas, were instilled through a bronchoscope into healthy volunteers. [This would be equivalent to 10 µg/M3 averaged over a work shift.] PM2.5 from both areas increased the number of white cells in the bronchoalveolar lavage performed 24 hours later. PM2.5 from the smelter area, but not the clean area, induced a significant influx of monocytes. Oxidant radical generation of bronchoalveolar lavage cells and cytokine concentration (interleukin-6 and tumor necrosis factor-alpha) in bronchoalveolar lavage fluid was significantly increased after instillation of Hettstedt PM2.5.

The invesgtigators concluded that environmentally relevant concentrations of PM2.5 from the smelter area induced distinct airway inflammation in healthy subjects with a selective influx of monocytes and increased generation of oxidant radicals. The higher concentration of transition metals in PM2.5 from smelter area might be responsible for this increased inflammation.

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Am J Respir Crit Care Med. 2004 Oct 15;170(8):898-903.

Metal-rich Ambient Particles (Particulate Matter2.5) Cause Airway Inflammation in Healthy Subjects

Frank Schaumann, Paul J. A. Borm, Andreas Herbrich, Johannes Knoch, Mike Pitz, Roel P. F. Schins, Birgit Luettig, Jens M. Hohlfeld, Joachim Heinrich and Norbert Krug

Fraunhofer Institute of Toxicology and Experimental Medicine, Hannover; Institut für Umweltmedizinische Forschung, Duesseldorf; and GSF-National Research Center for Environment and Health, Institute of Epidemiology, Neuherberg, Germany
Correspondence and requests for reprints should be addressed to Norbert Krug, M.D., Fraunhofer Institute of Toxicology and Experimental Medicine, Nikolai-Fuchs-Str. 1, Hannover 30625, Germany. E-mail: krug@item.fraunhofer.de